Search

Respiratory function has become a global health priority. Not only is chronic respiratory disease a leading cause of worldwide morbidity and mortality, but the COVID-19 pandemic has heightened attention on respiratory health and the means of enhancing it. Subsequently, and inevitably, the respiratory system has become a target of the multi-trillion-dollar health and wellness industry. Numerous commercial, respiratory-related interventions are now coupled to therapeutic and/or ergogenic claims that vary in their plausibility: from the reasonable to the absurd. Moreover, legitimate and illegitimate claims are often conflated in a wellness space that lacks regulation. The abundance of interventions, the range of potential therapeutic targets in the respiratory system, and the wealth of research that varies in quality, all confound the ability for health and exercise professionals to make informed risk-to-benefit assessments with their patients and clients. This review focuses on numerous commercial interventions that purport to improve respiratory health, including nasal dilators, nasal breathing, and systematized breathing interventions (such as pursed-lips breathing), respiratory muscle training, canned oxygen, nutritional supplements, and inhaled L-menthol. For each intervention we describe the premise, examine the plausibility, and systematically contrast commercial claims against the published literature. The overarching aim is to assist health and exercise professionals to distinguish science from pseudoscience and make pragmatic and safe risk-to-benefit decisions.

We hypothesized that severe hypoxia limits exercise performance via decreased contractility of limb locomotor muscles. Nine male subjects [mean [+ or -] SE maximum [O.sub.2] uptake ([Vo.sub.2max]) = 56.5 [+ or -] 2.7 ml*[kg.sup.-1]*[min.sup.-1]] cycled at [greater than or equal to] 90% [Vo.sub.2max] to exhaustion in normoxia [NORM-EXH; inspired [O.sub.2] fraction ([MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII.]) = 0.21, arterial [O.sub.2] saturation ([MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII.]) = 93 [+ or -] 1%] and hypoxia (HYPOX-EXH; [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII.] = 0.13, [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII.] = 76 [+ or -] 1%). The subjects also exercised in normoxia for a time equal to that achieved in hypoxia (NORM-CTRL; [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII.] = 96 [+ or -] 1%). Quadriceps twitch force, in response to supramaximal single (nonpotentiated and potentiated 1 Hz) and paired magnetic stimuli of the femoral nerve (10-100 Hz), was assessed pre- and at 2.5, 35, and 70 min postexercise. Hypoxia exacerbated exercise-induced peripheral fatigue, as evidenced by a greater decrease in potentiated twitch force in HYPOX-EXH vs. NORM-CTRL (-39 [+ or -] 4 vs. -24 [+ or -] 3%, P < 0.01). Time to exhaustion was reduced by more than two-thirds in HYPOX-EXH vs. NORM-EXH (4.2 [+ or -] 0.5 vs. 13.4 [+ or -] 0.8 min, P < 0.01); however, peripheral fatigue was not different in HYPOX-EXH vs. NORM-EXH (-34 [+ or -] 4 vs. -39 [+ or -] 4%, P > 0.05). Blood lactate concentration and perceptions of limb discomfort were higher throughout HYPOX-EXH vs. NORM-CTRL but were not different at end-exercise in HYPOX-EXH vs. NORM-EXH. We conclude that severe hypoxia exacerbates peripheral fatigue of limb locomotor muscles and that this effect may contribute, in part, to the early termination of exercise. hypoxemia; muscle fatigue; exercise performance

The effect of exercise-induced arterial hypoxemia (EIAH) on quadriceps muscle fatigue was assessed in 11 male endurance-trained subjects [peak [O.sub.2] uptake ([V.sub.[O.sub.2 peak]]) = 56.4 [+ or -] 2.8 ml*[kg.sup.-1]*[min.sup.-1]; mean [+ or -] SE]. Subjects exercised on a cycle ergometer at [greater than or equal to] 90% [V.sub.[O.sub.2 peak]] to exhaustion (13.2 [+ or -] 0.8 min), during which time arterial [O.sub.2] saturation ([Sa.sub.[O.sub.2]]) fell from 97.7 [+ or -] 0.1% at rest to 91.9 [+ or -] 0.9% (range 84-94%) at end exercise, primarily because of changes in blood pH (7.183 [+ or -] 0.017) and body temperature (38.9 [+ or -] 0.2[degrees]C). On a separate occasion, subjects repeated the exercise, for the same duration and at the same power output as before, but breathed gas mixtures [inspired [O.sub.2] fraction (F[I.sub.[O.sub.2]]) = 0.25-0.31] that prevented EIAH ([Sa.sub.[O.sub.2]] = 97-99%). Quadriceps muscle fatigue was assessed via supramaximal paired magnetic stimuli of the femoral nerve (1-100 Hz). Immediately after exercise at F[I.sub.[O.sub.2]] 0.21, the mean force response across 1-100 Hz decreased 33 [+ or -] 5% compared with only 15 [+ or -] 5% when EIAH was prevented (P < 0.05). In a subgroup of four less fit subjects, who showed minimal EIAH at F[I.sub.[O.sub.2]] 0.21 ([Sa.sub.[O.sub.2]] = 95.3 [+ or -] 0.7%), the decrease in evoked force was exacerbated by 35% (P < 0.05) in response to further desaturation induced via F[I.sub.[O.sub.2]] 0.17 ([Sa.sub.[O.sub.2]] = 87.8 [+ or -] 0.5%) for the same duration and intensity of exercise. We conclude that the arterial [O.sub.2] desaturation that occurs in fit subjects during high-intensity exercise in normoxia (-6 [+ or -] 1% [DELTA][Sa.sub.[O.sub.2]] from rest) contributes significantly toward quadriceps muscle fatigue via a peripheral mechanism. magnetic stimulation; low- and high-frequency fatigue; quadriceps twitch force; voluntary activation; peripheral fatigue; central fatigue